Coronary heart disease (CHD) or coronary artery disease (CAD) is the outcome of the atherosclerotic process in the coronary arteries in the heart.
Cardiovascular disease is the leading cause of death in this country. Within cardiovascular disease, CHD is the leading cause of death.
425,425 deaths in the United States in 2006 (about one of every six deaths)
1,255,000 new and recurrent coronary attacks per year
About 34 percent of people who experience a coronary attack in a given year die from it
One person dies every 33 seconds from CHD
The ischemic manifestation of CHD is angina or the equivalent whereas infarct is a Myocardial Infarction (MI).
Angina is typically described as squeezing, pressure, heaviness, tightness or pain in your chest. Many people with angina say it feels like someone is standing on their chest.
Angina, also called angina pectoris ("pectoris" means chest), may be stable or unstable:
Stable angina (persistent, recurring chest pain that usually occurs with exertion)
Unstable angina (sudden, new chest pain — or a change in the pattern of previously stable angina — that may signal an impending heart attack)
A third, a rare type of angina called variant angina (also called Prinzmetal's angina) is caused by a coronary artery spasm.
Angina is relatively common, but can be hard to distinguish from other types of chest pain, such as the pain or discomfort of indigestion. If you have unexplained chest pain, seek medical attention right away.
Ischemic or non-Angina symptoms include:
Nausea
Fatigue
Shortness of breath
Anxiety
Sweating
Dizziness
A woman's angina symptoms can be different from the classic angina symptoms. For example, a woman may have chest pain that feels like a stabbing, pulsating or sharp form of chest pain rather than the more typical vise-like pressure. Women are also more likely to experience symptoms, such as nausea, shortness of breath or abdominal pain. These differences may lead to delays in seeking treatment.
The severity, duration and type of angina can vary. Angina, unresponsive to rest or nitroglycerine and lasting >15 minutes is an Infarct.
The etiology of coronary artery disease is the atherosclerotic process. The sites for advanced lesions are found more in the branch points of the coronary arteries.
There are three conduit arteries in the myocardium.
Right Coronary Artery (RCA)
Left Anterior Descending (LAD)
Circumflex
These arteries originate at the base of the aorta through the RCA and left main artery. The left main divides into the LAD and circumflex. Each of these arteries supply different areas and function of the heart; although areas sometimes overlap.
Right Coronary Artery
Left Anterior Descending
Circumflex
1/3 Intraventricular Septum
Right Ventricle
AV Node
Atrial Septum
Ventricular Septum
Parts of the Left Ventricle
Anterior Ventricle
2/3 Anterior Septum
Anterior Apex
Bundle of His
Bundle Branches
Left Lateral Ventricle
Left Atrium
Ventricular Septum
When clinical lesions are found in specific coronary arteries, ischemia or infarct results. Cardiac function in these specific areas is then compromised. Cardiac function is measured by
Electrical Activity
Cardiac Performance
Ejection Fraction
Wall Motion
The function of the heart depends on the size of the lesion and the subsequent blood flow. When the supply<demand, ischemia exists. The figure below illustrates the relationships between myocardial blood flow (supply) and the work of the heart (demand).
The x-axis is the demand; whereas the y-axis is the supply.
The normal supply:demand relationship is illustrated in red. As the demand for work increases, the blood flow accommodates
The blue line shows how the relationship changes when the artery has a 50% lesion.
A 70% lesion will compromise blood flow during exercise. 70% or greater lesions are usually bypassed.
Can the atherosclerotic plaque be reversed once it is well established in the wall of the artery?
Regression of atherosclerotic plaque is defined as any of the following:
lumen size is increased
endothelium is repaired
decreased amounts of intimal proliferation
decreased number of cells in the intima
decreased intracellular and extracellular lipid
no areas of necrosis or calcification at the primary disease site
Sylvester and colleagues approached this topic as a lack of disease progression. They followed 104 cardiac patients and divided them up into
sedentary - no activity (n=36 patients with 47 vessels)
low - one session/week (n=20 patients with 51 vessels)
moderate - 1-2 sessions per week (n=20 with 35 vessels)
high - >3 sessions per week (n=9 patients with 16 vessels)
physical activity groups.
They performed cardiac caths 20 months apart. They defined progression as >30% greater occlusion.
The figure on the right illustrates the percentage of vessels that progressed during this time.
These groups were not randomized. That is, the patients were classified into the physical activity groups based on their regular physical activity habits. Thus, the selection vs protection issue applies to this study; similar to an epidemiological study.
Selvester, R., J. Camp, and M. Sanmarco. Effects of exercise training on the progression of documented coronary arteriosclerosis. The Marathon: Physiological, medical, epidemiological and psychological studies. Annals of New York Academy of Science 301: 495-508, 1977.
Haskell and colleagues have the classic study on progression of coronary artery disease with intensive risk factor reduction, which included exercise. In this study, 300 patients were randomized into usual care (control group) and risk factor reduction groups. Cardiac categorizations and cardiac events were measured over a period of four years.
Haskell, W.L., E.L. Alderman, J.M. Fair, D.J. Maron, S.F. Makey, R. Superko, P.T. Williams, I.M. Johnstone, M.A. Campagne, R.M. Krauss, and J.W. Farquhar. Effects of intensive multiple risk factor reduction on coronary atherosclerosis and clinical cardiac events in men and women with coronary artery disease: The Stanford Coronary Risk Intervention Project (SCRIPT) Circulation 89:975-990, 1994.
The figure on the left illustrates the change in artery diameter after four years.
The Usual Care group exhibited a greater reduction in the artery diameter than the Risk Reduction group.
The conclusion was the Usual Care group exhibited greater disease progress than the risk reduction group.
This is also illustrated in the percent stenosis of the arteries.
The Usual Care group exhibited a greater stenosis (closure) of the coronary arteries after the four year period.
This is also reflected in the number of events over the four year period.
The Risk Reduction group had fewer cardiac events.
An interesting finding from this study was the arteries that were between 40-60% blockage were the most likely to be the source of cardiac events.
Hammond, K. Regression of atherosclerosis - A review. Journal of Cardiac Rehabilitation 3:347-359, 1983.
Hammond found 32 patients out of 143 from 11 studies had documented disease regression in 1983. Six of the studies targeted the coronary arteries; four the femoral artery; and the other one targeted the aorta and renal arteries. Only one of these studies utilized exercise as an intervention. The rest used cholesterol lowering drugs, plasma exchange, renal bypass, and diet.
Hammond proposed a cholesterol exchange model based on influx and efflux:
Most of the research on regression has been with interventions other than exercise.
The figure to the left illustrates the percent of patients who exhibited regression of atheroma in the coronary arteries with multiple drug therapies.
The primary meds were
Colestipol
Niacin
Lovastatin
CLASS = Cholesterol lowering Atherosclerosis Study
FATS = Familial Atherosclerosis Treatment Study (New England Journal of Medicine 323:1289-1298, 1990)
SCOR = Specialized Center of Research Intervention Trial (JAMA 264:3007-3012, 1990)
HARP = Harvard Atherosclerosis Reversibility Project (Lancet 344:1182-1186, 1994)
Can exercise be effective in prevention and treatment of coronary artery disease?
The classic epidemiological studies show an inverse relationship between physical activity and coronary artery disease. Powell & Berlin summarized these epidemiological studies.
Powell and colleagues reviewed 121 articles reporting on 54 different epidemiological studies on physical activity and coronary artery disease. He found 43 of the studies to be of sound scientific design. In these studies physical activity was measured by
occupational physical activity
occupational and leisure physical activity
stairs climbed & city blocks walked
sport activity
Some of these classic studies included:
London postal workers vs civil servants
London transport busmen
Los Angeles civil servants
Bell Telephone employees
US Railroad workers
Chicago Utility Company employees
San Francisco Longshoremen
Harvard Alumni
Framingham Study
Gothenburg Sweden residents
In his summary of these articles:
an inverse association between physical activity and incidence of coronary artery disease was consistently observed
the better designed/controlled studies had the stronger results
the relative risk of inactivity is just as strong as
hypertension
smoking
hypercholesterolemia
Berlin and colleagues completed a similar study three years later and found the same results. They reported a two times lower risk for coronary artery disease for individuals who were physically active.
Blair and colleagues conducted another epidemiologic study with over 32,000 subjects in 1996. This time they observed the relationship between cardiovascular disease and cardiorespiratory fitness instead of all-cause mortality. The findings were not different from the all-cause mortality data. That is, the lowest risk of cardiovascular disease was found for the highest fitness category and the highest
risk was found for the lowest fitness category, despite the other risk factors. The relative risk of low fitness (2.03) was just as strong, if not stronger than
smoking (1.89)
hypertension (1.67)
hyperlipidemia (1.45)
family history (1.24)
overweight (1.33)
elevated glucose (1.63)
abnormal ECG (2.05)
Risk of cardiovascular disease is not the only variable that decreased with increasing fitness. The lifestyle variables of cholesterol, blood pressure, body mass index, and glucose showed the same pattern. That is, high fitness was associated with lower cholesterol, blood pressure, body mass index, and glucose whereas low fitness was associated with higher cholesterol, blood pressure, body mass index and glucose. Even with those variables that are not affected by exercise, like family history and smoking, the risk of disease was lower in each of these categories as fitness increased. That is, even though family history increases the risk of disease, exercise can reduce that risk.
Because the epidemiological research demonstrates strong findings, it would seem that the clinical trials in heart disease prevention would be even more definitive. However, the clinical trials conducted with human subjects have not been well controlled and cannot provide needed information.
The first clinical trial on humans was the Tri-State Study in the late 1960s. In this study 209 men were presented with exercise treatment to prevent heart attacks and 176 served as controls. The University of Minnesota, University of Wisconsin and Penn State were the sites for the interventions. The exercise at each of these sites was not consistent. The primary problem with the study was the dropout from exercise which was greater than 50%. This dropout compromised any conclusions the researcher could make regarding the effects of exercise in the prevention of coronary heart disease.
The figure to the right illustrates the cholesterol reduction in the Tri-State Study for the control and exercise groups.
Both groups decreased cholesterol similarly. This decrease in cholesterol cannot be attributed to exercise.
Although the 1985 follow-up of the Tri-State Study, demonstrated a significant inverse relationship between exercise and coronary heart disease, it was not different in design from an epidemiologic study.
MacKeen, et al. A 13 year follow-up of a coronary heart disease risk factor screening and exercise program for 40-59 year old men: Exercise maintenance and physiologic status. Journal of Cardiopulmonary Rehabilitation 5:510-523, 1985.
The most famous clinical trial was the Multiple Risk Factor Intervention Trial (MR FIT Study) in the late1970's. It was designed provide multiple intervention to lower blood pressure, stop smoking, and alter dietary habits to lower cholesterol. Exercise was part of the intervention. As in a good clinical trial, subjects were randomized into Usual Care (control) and Intervention groups.
However, by the late 1970's, there was enough popular information on how to lower blood pressure, stop smoking, and lower cholesterol. Seems like the control group did just as well as the intervention group in lowering these risk factors as well as in exercising. No additional information was contributed by these clinical trials on humans.
The graph to the left illustrates the six year mortality data for both groups. The intervention was not successful in that it was not different from the usual care group. There were no statistical differences in the death rates between the two groups.
The focus of the prevention research in humans changed from observing heart disease mortality as the important outcome to the effects of exercise on the separate risk factors with the concept that reducing the risk factors would reduce the incidence of disease.
The best clinical trial data comes from animal studies such as this monkey study. In 1981, Kramsch and colleagues studied 27 monkeys for 36 months. Nine monkeys ate an atherogenic diet and exercised on monkey treadmill (the Ex-Athero group). Nine ate an atherogenic diet, but did not exercise (the Sed-Athro Group). Nine more ate a nutritionally balance diet and did not exercise (the Sed-Norm group).
The exercise group (Ex-Athro) had larger arterial lumen, smaller atherogenic lesions, and less narrowing of the coronary arteries than the sedentary monkeys, whether on the atherogenic diet or not.
Thus, as a well-controlled clinical trial, this animal study adds more information. Kramsch and colleagues found a lower incidence of disease, confirmed by physiological evidence, in exercising monkeys, even on an atherogenic diet.
How effective is physical activity in the treatment of coronary artery disease?
Physical work capacity increases in just about every cardiac patient. VO2max can increase as high as 50% in the cardiac population because their VO2max was extremely low to begin. In the non-cardiac patient, VO2max increases primarily due to an increase in stroke volume. Can the same mechanism improve VO2max in the cardiac patient?
LeMura and colleagues summarized the research studies that measured VO2max and possible mechanisms of change. In 1990, there were 20 studies (444 subjects) that investigated whether the improvement in VO2max in cardiac patients was due to central or peripheral mechanisms.
Central mechanisms would be an increase in stroke volume and subsequent cardiac output. Peripheral mechanisms include increase in (a-v) O2difference or oxygen extraction at the tissue level.
VO2 = Cardiac Output x (a-v) O2 difference
It turns out 10 of the 20 studies (50%) found central mechanisms and 10 found peripheral mechanisms.
These tables summarize the characteristics of the studies finding central adaptations and those finding peripheral adaptations.
Physical work capacity can be increased by either central or peripheral mechanisms.
The extent of the myocardial damage was not a factor in central vs. peripheral changes. Central changes may be more influenced by high intensity exercise.
Oxidative enzymes, myofiber type and size were measured to confirm peripheral changes whereas myocardial contractility, perfusion, ejection fraction, stroke volume, left ventricular performance, and double product at angina threshold represented the variables of central changes.
Froelicher's study utilizing ventricular function in 16 cardiac patients was included in LeMura's review. In reality, Froelicher reported on the 16 patients who exhibited central changes out of 300 patients who did not change central cardiac function.
For the most part, we tell patients we cannot change ventricular function for the damaged parts of the heart.
CAN EXERCISE TREAT THE SYMPTOMS OF CORONARY ARTERY DISEASE?
The primary symptom of coronary artery disease is angina (ischemia). Angina is often evaluated with exercise stress testing where a progressive increase in exercise intensity is presented to the patient. The workrate where angina occurs is called the angina threshold.
Ferguson and colleague trained 10 patients with angina on cycle ergometry for 30 min/session for six months. Angina threshold increased 38%, however, no other cardiac variable was associated with it.
heart rate
systolic blood pressure
heart work
coronary blood flow
left ventricular oxygen uptake
coronary (a-v) O2difference
Angina threshold can also be predicted by double product (heart rate x systolic blood pressure). Even though the angina threshold increased for work rate, double product at its onset does not change. How can this happen? The cardiac patient becomes more efficient in ability to do the work. That is, peripheral changes can occur to improve work rate, but not alter central factors such as heart rate and blood pressure at the onset of angina.
Oldridge and colleagues summarized ten clinical trials for the effectiveness of cardiac rehabilitation on morbidity and mortality. These ten studies totaled 2145 control patients and 2202 rehabilitation patients. The programs ranged 6 weeks to 48 months. All of the programs included exercise as the primary mode of rehabilitation.
The figure to the left illustrates lower all cause mortality and cardiovascular death for the rehabilitation (treatment) groups.
The number of nonfatal infarctions is higher for the rehabilitation (treatment) groups; this means that survival increases with rehabilitation.
O'Connor and colleagues completed a similar study the next year. He found 22 randomized clinical trials of cardiac rehabilitation involving 4,554 patients. These studies ranged over three years. The three year data is reported in the figure to the below.
The data were divided into programs that included all types of rehab (n=21), those that were exercise alone (n=6), and those that used exercise + other types of rehabilitation. These data are reported as Odds Ratios which compares the treatment group to 1 or the red dotted line. The data below the red dotted line means less incidence of the event.
To summarize both of these studies, rehabilitation, including exercise:
20% decrease in mortality
20% decrease in morbidity
To summarize the effectiveness of exercise treatment of coronary artery disease.
The types of patients in cardiovascular disease include:
Dyslipoproteinemia
Angina
Myocardial Infarction
Sudden Death
Congestive Heart Failure
Dysrhythmia
The components of clinical management include evaluation and treatment of CAD.
The purpose of the evaluation includes:
diagnosis of disease (Dx)
prognosis of disease
size and location of ischemia or infarct
performance of the heart
ejection fraction
wall motion
Whereas the purpose of treatment is to eliminate the symptoms. Because the symptoms occur because of an imbalance between supply and demand, treatment focuses on either increasing the supply or decreasing the demand.
The most common types of evaluation and treatment are summarized below:
The basic physical examination includes questioning on symptoms, specifically angina or angina equivalents, listening to heart and breath sounds, evaluating murmurs, listening to (bruits) sounds over the carotid artery, blood pressure, BMI, cholesterol, and taking a 12 lead electrocardiogram.
A chest X-Ray may be included in the physical exam to evaluate the size of the heart and ventricle.
CARDIAC CATHERIZATION
The heart catheterization provides information on
arterial location of the lesions
size of the occlusions
percentage closure of the artery
ejection fraction
A catheter is inserted in the femoral artery and led to the origin of the aorta which is the also the origins of the coronary arteries.
A dye is then injected in the origins of the coronary arteries.
The dye is imaged by the motion x-ray as the dye passes through the arteries.
The narrowing of the silhouette of the artery (arrow to the left) indicates an atherosclerotic lesion that has occluded the artery.
Thus, the cardiac catheterization locates the artery blockage and the size of the blockage.
Results may be summarized as:
xx% blockage of a specific artery
distal or proximal
diffuse or focal
If ejection fraction is also measured during the cath, the performance of the heart can be evaluated. However, if the ejection fraction is not measured, the cath does not evaluate
the area of the heart that is truly affected by the blockage
the cardiac performance that may be compromised by the blockage
CORONARY COMPUTED TOMOGRAPHY ANGIOGRAM (CTA)
CTA is a newer technology to assess the coronary arteries. It used advanced CT technology with a contrast material (dye) to obtain a high-resolution, three dimension images of the beating heart and the conduit vessels. CTA, like the cardiac cath, is performed during rest.
A contrast dye is injected through a vein while the heart is imaged through the CT scanner.
The X-ray tube and detectors rotate around the patient making three dimension images of the body. In the cardiac CT scan, the images are associated with the heart beat.
Pictured here are cross-sectional cuts of the vessels (left panels) showing occlusions similar to the cath.
Whereas these images show calcification without blockage.
NUCLEAR CARDIOGRAPHY
The nuclear cardiography provides the information not included in the cardiac catheterization.
Nuclear cardiography involves the injection of a radioactive material that can be detected with a gamma counter or CT scanner.
The radioactive tracer is either injected into the vein or combined with the red blood cells during the procedure, then scanned to determine it's distribution.
The distribution of the radioactive tracer can provide information on
size and location of infarct
infarct vs. ischemia
myocardial performance
myocardial metabolism
Technetium Heart Scan
The Technetium Heart Scan is given after (within 12 hours) an MI to determine the size and location of the necrotic tissue. Technetium (Tc99) is the radioactive tracer that is injected 2-3 hours before the heart is scanned so that the tracer will settle in the necrotic heart tissue. A Gamma counter then picks up the gamma emissions from the Tc99 indicating the necrotic tissue.
A "hot spot" is considered tissue that is necrotic thus indicating the size and location of the infarct.
Nuclear Perfusion Studies
There are several types of Nuclear Perfusion Studies. For the most part, the purpose is to determine the difference between ischemic and necrotic tissue. All nuclear perfusion studies involve the stress test. However, if the patient cannot perform exercise, the exercise increase in heart rate will be simulated by pharmacology.
Adenosine
Dobutamine
Diprymamol
Thallium (Tl201) or Cardiolite or Sestimibi are used as the radioactive tracers in Nuclear Perfusion Studies. These radioactive tracers seek out perfused tissue. That is, tissue that receives a blood supply. Tissue that is not necrotic.
The protocol for nuclear perfusion studies is to walk upright on a treadmill to about 85% of HRmax. Near the end of the test, the radioactive tracer is infused by IV.
Immediately after exercise the patient is supine in the gamma counter for the first scan.
120 minutes following the exercise, the patient goes back into the counter for a second scan.
Since these radioactive tracers seek out perfused tissue. Because the "hot spot" is good living tissue, nuclear perfusion studies is often called the "cold spot" imaging.
The illustration to the right shows the different angles of the images.
Comparisons are made between the two scans; immediate post and 120 min rest.
In the immediate post stress test images on the top of this scan, there are areas of the myocardium that do not exhibit hot. These "cold spot" area are then considered areas of low or no blood flow.
To distinguish whether these areas are ischemia or infarct, the second image is compared to the first.
In this case, those areas that were "cold spots" are now filled in on the bottom rest images (120 min post). Because these spots turned from "cold" to "hot" it means that the area became re-perfused and are not necrotic. Thus, they were ischemic areas.
If the "cold" spots remain "cold" the areas are infarcted or necrotic area.
Interpretation of the nuclear perfusion studies are based on the 120 min image:
reprofused (ischemic)
fixed (infarct)
In addition to determining whether the area of the heart is ischemic or necrotic, the images can also provide information on the size and location of the damaged tissue.
PET
The PET scan is similar to the nuclear perfusion scan in terms of detecting areas of perfusion. However, exercise is not used in the PET scan. The PET scan can also show the heart during work; whereas the nuclear perfusion studies produce still images collected over several heart beats.
Fluorodeoxyglucose (FDG) = glucose + Fluorine (FL18) is the tracer used in PET scans. Occasionally, glucose is infused with the fluorine. PET (gamma) scans are made of the heart before and after infusion of the radioactive tracer. In some cases, the gamma scanner is combined with a CT or MRI scanner; and both scans are done simultaneously.
The image from the PET scan is similar to the image from nuclear perfusion studies. The image, however, reflects metabolically active tissue. The tissue cannot be metabolically active without a blood supply.
MUGA
The PET and the Nuclear Perfusion Scan both indicate the size and location of ischemia or infarct. However, how does these defects affect the performance of the heart? Can the heart still pump blood adequately?
Technetium (Tc99m) is the radioactive tracer used in MUGA studies. In these tests, the Tc99m tags the red blood cell which makes the blood volume visible to the gamma counter. With the blood tagged with the tracer, the images indicate the blood flow through the chambers of the heart.
Exercise is also utilized in MUGA studies to stress the heart. However, the exercise is supine leg ergometry.
Blood is removed and tagged withTc99m. This blood is given back to the patient.
The camera images the heart at peak exercise and recover. Each still image taken is combined to make a moving picture of the wall of the heart and to evaluate ejection fraction.
The motion of the heart is coordinated by the heart rate. The ECG is taken along with the imaging. The computer organizes the images to take about 13 to 17 images for each heart beat; and then combines these images to represent several contractions.
Thus, the name, MUltiple Gated Acquisition.
A moving picture of heart beats is then analyzed for cardiac performance. The radioactive blood is counted by the gamma counter and converted to blood volume.
To measure the ejection fraction, the end systolic volume (emptiest; right illustration) is subtracted from the end diastolic volume (fullest; left illustration) and divided by the end diastolic volume; and multiplied by 100 to obtain a percentage of the heart volume (cardiac output) that is ejected.
A normal ejection fraction is 50-60%.
At the same time, the wall motion can be analyzed. Remember the computer only sees the radioactive material. The computer makes an outline of the walls of the chambers using the volume of blood in each chamber. The movement of each wall can then be observed.
Echocardiography is the ultrasound images of the heart's anatomy. Originally, echocardiography was utilized to observe valves and great vessels in real time. Now, with technology, echocardiographic images can also exhibit myocardial performance characteristics. Cardiac echocardiography has included:
The heart is viewed on the computer screen as the ultrasound transducer is moved across the chest.
Different positions provide different aspects of the heart.
Four basic views are taken (see below)
Similar to the MUGA the volume of end systole can be compared to the volume at end diastole to calculate ejection fraction.
Wall motion can observed directly.
In the stress echo, the patient exercises to 85% HR max on a treadmill. As soon as exercise is over, the patient is transferred to the cot where the echo images the heart.
If the patient cannot exercise, the heart rate and contractility of exercise is simulated with medications.
In some cases, a Transesophogeal Echo (TEE) is used to see myocardial structures closer than in the transthorasic echo.
A transducer is inserted down the esophagus to image the heart.
No matter what type of treatment is incorporated for each patient, the goal of the treatment is balance the supply vs. demand equilibrium of the coronary arteries; either by increasing the supply or decreasing the demand, or both.
The types of patients found in exercise programs include:
Dyslipoproteinemia
Angina
Myocardial Infarction
Sudden Death
Congestive Heart Failure
Dysrhythmia
MEDICAL & SURGICAL TREATMENTS
Medical treatment is use of pharmacology and lifestyle changes. Whereas surgical treatment include
In the PTCA procedure a small balloon is introduced to the blocked artery and inflated to open the blockage. Although the PTCA is an invasive procedure, the hospital stay is only 2-3 days. A discharge stress test may be given with a follow-up in 2 weeks. Exercise is not initiated until 6-8 weeks post; although a walking program is usually encouraged at discharge.
With the aid of cardiac catheterization results, the location and percent blockage of each artery is known.
Similar to the cardiac catheterization, the balloon is passed up through the large arteries of the leg to the origins of the coronary arteries.
The catheter is then inserted in the coronary artery at the location of the lesion. The balloon is inflated to open the blockage.
The primary risk of PTCA is closure of the artery, or restenosis. Approximately 30-40% of patients have restenosis within six months of the PTCA.
To prevent restenosis, a stent (lower left) is placed in the artery. This stent not only keeps the artery patient, but may also contain an anticoagulant.
An Atherectomy may also be done at the time of the angioplasty. Fatty deposits and plaque are shaved away from the wall of the artery.
Vascular endothelial growth factor (VEGF) is also applied to help repair the endothelium.
CORONARY ARTERY BYPASS GRAFT (CABG)
The CABG utilizes a vein or artery to bypass the lesion; thus, supplying blood down-stream from the lesions. Lesions > 75% occlusion are candidates for bypass. This procedure requires open heart surgery to view the heart. Hospital stay is 3-8 days; first two in intensive care. A Physical Therapist, nurse, or Registered Clinical Exercise Physiologist will begin exercise as an inpatient within 18 hours after open heart surgery.
The first bypasses were performed using the saphenous vein from the leg. (left) More recently, veins from the arm have been used.
If the number of vessels needing bypass is low, the internal mammary artery can be used. (right)
MINIMALLY INVASIVE DIRECT CORONARY ARTERY BYPASS
The Midcab is utilized with high-risk patients who require only 1-2 lesions bypassed. The internal mammary artery is used. The procedure is only 3 hours vs the six of traditional CABG. The recover is shorter; from months to days or weeks.
A laser is introduced into the chamber of the heart similar to the procedures for the heart cath. The laser then drills holes in the myocardium to increase blood supply to the muscle. A total of 20-40 channels are created.
During the clinical event, thrombolytic therapy and restoring perfusion are primary pharmacological goals. The more long-term goal of pharmacology specific to coronary artery disease is to counteract ischemia. These medications target the supply-demand function of the heart. Other medications are given to treat the risk factors; we will present those medications in later sections of hypertension and hyperlipidemia.
Anti-anginal Medications
Nitroglycerine
Beta Blockers
Ca++ Channel Blockers
NITROGLYCERINE (NTG) is a vaso-veno dilator. NTG functions similarly as nitric oxide, however it's action is directly on the smooth muscle, bypassing NO production. NTG primary effects on coronary blood supply in vasodilation of the coronary arteries; minor effects on the supply include an decrease in ejection time because of an increased heart rate. On the demand side, NTG decreases demand by decreasing ventricular volume and ventricular pressure. Ventricular volume is decreased because of venodilation in the systemic system. Blood pooling in the venous system decreases venous return; hence decreases ventricular volume. Vasodilation in the systemic vasculature also decreases ventricular pressure required to overcome the afterload. NTG primary effects on the supply:demand relationship is to decrease demand.
NTG can be short (<1 hr) and long acting (3-4 hrs). Short acting NTG is given when angina presents. Long acting NTG is taken to prevent angina.
NTG can be taken:
Oral
Chewable
Topical
Patch
Toxicity to NTG presents as vascular headache and orthostatic hypotension. Hypotension following exercise is also a risk.
NTG increases angina threshold and physical work capacity. Angina threshold presents at a higher double product, however, primarily due to the decreased ejection time and the increased heart rate.
BETA-BLOCKERS block the beta-adrenergic receptors; thus blocking adrenergic (norepinephrine & epinephrine) stimulation. Beta-blockers are also called beta-adrenoceptor antagonists. Beta-blockers are given for:
anti-anginal
anti-hypertensive
anti-arrhythmias
There are three types of Beta-blockers:
General or Non-Selective
Cardio-Selective
Cardio-Selective with Intrinsic Sympathomimetric Activity (ISA)
Type of Beta-Blocker
Primary Cardiovascular Actions
Non-selective Beta-blockers work on both the beta1 and beta2-adrenergic receptors throughout the body. Because insulin production and secretion, as well as bronchodilation involves non-selective beta-adrenergic receptors, beta-blockade decreases insulin production and secretion and results in bronchoconstriction.
decrease heart rate
decrease contractility
decreases conduction velocity
Cardio-Selective Beta-Blockers only block the Beta1 receptors in the heart.
decrease heart rate
decrease contractility
coronary vasoconstriction
decreases conduction velocity
increase ejection time
Cardio-Selective Beta-Blockers with Intrinsic Sympathomimetric Activity are partial agonists as background sympathetic activity is maintained, while normal or enhanced activity is prevented.
decrease heart rate
decrease contractility
systemic vasodilation
decreases conduction velocity
The primary effect on the balance of supply and demand is a decrease in demand. Supply is decreased by coronary vasoconstriction and a decreased by extended ejection time. However, the reduction in demand is much greater than the decrease in supply.
Similar to the nitrates, angina threshold is increased. However, the double product at angina threshold is lower on Beta-blockers; because of the decrease in coronary supply.
When angina threshold is increased, physical work capacity is as well. Physical work capacity on Beta-blockade is limited to angina patients only.
Precautions during exercise on Beta-blockade include hypotension in recovery. Other precautions exist for non-anginal patients.
Ca++ CHANNEL BLOCKERS bind to the L-type calcium channels (long lasting) located in the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue. Obviously Ca++ channel blockers block the influx of Ca++ into the cell, thus blocking actions caused by Ca++; muscle contraction. That is, muscle contraction of the smooth muscle in the vasculature, cardiac myocytes and cardiac nodal tissue.
Ca++ channel blockers are given for:
anti-anginal
anti-hypertensive
anti-arrhythmias
There are three types of Ca++ channel blockers:
dihydropyridines
non-dihydropyridines
phenylkylamine
benzothiazepine
These classes of Ca++ channel blockers differ by their selectivity for vascular or cardiac Ca++ channels.
Type of Ca++ Channel Blocker
Primary Cardiac Actions
dihydropyridines
high vascular selectivity
vasodilation
phenylkylamines
myocardial selectivity
decreased contractility
benzothiazepines
cardiac depressant
vascular vasodilator
When Ca++ channel blockers are used as anti-anginal meds, the demand side of the supply:demand balance is reduced; angina threshold is increased, physical work capacity is increased, and double product remains unchanged at angina threshold.
Above: A summary of how anti-anginal meds affect the supply vs. demand relationship of the heart.
Inpatient caridiac Rehab is the exercise/physical activity provided while the patient is in the hospital. The purpose of inpatient activities are
Counteract the effects of bed rest
Psychological outlook
Earlier hospital discharge
Inpatient begins in the critical care unit within 1-2 days post event, 2-4 days if the event is complicated; and 18 hours after open heart surgery.
MODE
Self care
Range of Motion
Posture
Walking
Stair Climbing
Circuit Training
FREQUENCY
Early mobilization 3-4.day (days 1-3)
Later mobilization 2/day (beginning on day 4)
DURATION
Intermittent sessions 3-5 min
Total duration up to 20 min
INTENSTIY
RPE <13
Post MI: HR <120/min or +20/rest
Postsurgery +30/rest
Symptomatic
PRECAUTIONS
Depending on condition and procedure
RECOMMENDATION
Outpatientcardiac rehabilitation is for patients who come back to the hospital to exercise. The purpose of outpatient rehab
regain function
return to work
The components of outpatient rehab are
Exercise
Education
Support
58% begin outpatient rehab immediately after discharge
24% begin 2-4 weeks after
18% begin 6-12 weeks after
In exercise, the patients return to the hospital three days a week for a 40-60 min exercise session. Their blood pressure and ECG are monitored throughout the exercise session. The exercise consists of circuit of cycling, walking, stepping, and muscle endurance activities.
A home program is prescribed along with the outpatient rehab for the other days of the week.
The education and support session meet weekly or monthly. Topics for education include:
•High Blood Cholesterol
•Heart Health Nutrition
•Risk Factors for Heart Disease
•Exercise for a Healthy Heart
•Weight Control
•Smoking Cessation
•Understanding and Treating Heart Disease
•Stress Management
OUTPATIENT EXERCISE PROGRAM
MODE
Cardiovascular Circuit
Activities of Daily Living
Resistance - endurance
FREQUENCY
3/week
DURATION
30-40 min
10-20 min
INTENSTIY
70-85%
1 set
10-15 reps
8-10 exercises
PRECAUTIONS
Depending on condition and procedure
RECOMMENDATION
Smoking Cessation
Stress Management
Diet/Nutrition
The Home Exercise Program is prescribed both at discharge and during the Outpatient program. The home program consists entirely of walking and activities of daily living. The intensity is often guided by a list of activities that are representative of a MET expenditure.
HOME EXERCISE PROGRAM
MODE
Walking
Activities of Daily Living
FREQUENCY
4-5/week
DURATION
20-30 min
INTENSTIY
Discharge
Intensity of Inpatient (METs)
Outpatient
Intensity less than Outpatient (METs)
PRECAUTIONS
Depending on condition and procedure
RECOMMENDATION
Smoking Cessation
Stress Management
Diet/Nutrition
Maintenance Program is designed to prevent the next myocardial infarction. Maintenance programs range from supervised programs to individual programs at home or other facilities. Exercise prescriptions will be more specific, based on comorbidities.
MAINTAINENCE EXERCISE PROGRAM
MODE
Walking
Cardiovascular
FREQUENCY
3-5/week
DURATION
20-60 min
INTENSTIY
70-80%
PRECAUTIONS
See below
RECOMMENDATION
Smoking Cessation
Stress Management
Diet/Nutrition
Precautions for each type of patient are
PATIENT
PRECAUTIONS
Angina
monitor signs & symptoms of angina or angina equivalent
use nitroglycerine when angina presents
may become hypotensive after taking nitro
Beta blockers will have a lower HR and BP response
PTCA
restenosis possible
watch for signs & symptoms of angina or angina equivalent
CABG
watch for signs & symptoms of angina or angina equivalent
Dysrhythmia
report skipped beats in recovery
Pacemaker
slow warm-up and cool down
avoid extreme upper body extremity movements or anything hitting the pacemaker
AICD
keep heart rate under defibrillator rate
notify physician if discharged
Congestive Heart Failure
watch for signs & symptoms of angina or angina equivalent
watch for sudden weight gains
may be on diuretics: keep potassium normal
if on digitalis, look for digitalis toxicity (heart dysrhythmias)
